interleukin-8 and Paranasal-Sinus-Diseases

A component of primary innate defense of the nasal mucosa against inhaled pathogens includes continuous, low-level release of hydrogen peroxide (H2 O2 ) into luminal secretions. Epidemiologically, an association exists between poor air quality and increased prevalence of sinonasal disease. To understand the effects of particulate matter (PM) in nasal mucosa, we studied the release of H2 O2 and interleukin 8 (IL-8) after PM exposure.. Human nasal specimens were collected from surgery and cultured in serum-free growth medium. Cell integrity and recovery during culture was monitored by lactate dehydrogenase (LDH) release into the medium. Cultures were exposed to PM for 24 hours in the presence/absence of diphenyleneiodonium sulfate (DPI; a nicotinamide adenine dinucleotide phosphate [NADPH] oxidase inhibitor). Luminex cytokine and Amplex-Red H2 O2 assays were performed.. LDH levels dropped rapidly within 2 days, indicative of stabilization and cell recovery after harvest. All cultures released H2 O2 into the medium. Exposure to PM (20 μg/cm(2) ) increased H2 O2 levels significantly (94.6 ± 7.7 nM) compared to untreated controls (55.8 ± 4.0 nM; p = 0.001). PM-induced H2 O2 production was partially inhibited by DPI (80.1 ± 3.8nM), indicating that cellular NADPH oxidase may be a primary source of H2 O2 production. Exposure to PM increased IL-8 levels in a dose-dependent fashion (control = 2301 ± 412 MFI; 20 μg/cm(2) = 5002 ± 1327 MFI; 40 μg/cm(2) = 8219 ± 1090 MFI; p = 0.022).. PM increases the quantity of H2 O2 released by nasal epithelial cells, indicating that PM can contribute to oxidative stress in part by activating a normal cellular defense mechanism. Exposure to PM resulted in elevated IL-8 levels and mucin production in explants. Efforts to reduce airborne PM may lead to reduced H2 O2 and mucin production in sinonasal epithelium.

Topics: Adult; Cells, Cultured; Female; Humans; Hydrogen Peroxide; Immunity, Innate; Interleukin-8; L-Lactate Dehydrogenase; Male; Middle Aged; Models, Biological; Mucins; NADP; Nasal Mucosa; Onium Compounds; Paranasal Sinus Diseases; Particulate Matter; Prevalence; Primary Cell Culture

Symptoms of nasal, pharyngeal and ocular discomfort have been reported among workers in the wood surface-coating industry. Symptoms were reported more often by workers using ultraviolet radiation-curable acrylate coatings (UV coatings), which contain potential chemical sensitizers, than by those using acid-curing coatings. Furthermore, increased levels of eosinophil cationic protein (ECP) and albumin, but not tryptase, in nasal lavage from workers exposed to UV coatings have been observed. To further examine whether air contaminants present in the UV-coating industry are causing the observed increase in symptoms, the inflammatory process in the nasal mucosa of workers exposed to UV coatings was investigated. Clinical and biochemical endpoints were selected to distinguish between specific and non-specific hypersensitivity and to test the hypothesis that the symptoms were consistent with Type IV hypersensitivity. The nasal lavage and nasal biopsy were performed under local anesthetic at the workplace during working hours after a minimum of 2 h of work in both the exposed and control groups. Albumin and ECP, and the cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8), were used as inflammatory markers. A multi-probe ribonuclease protection assay was used to attempt to detect cytokine variation in human nasal biopsies. The cytokine genes analyzed were TNF-alpha, GM-CSF, interferon-gamma, IL-2, IL-4 and IL-5. L32 and GAPDH were used as control genes for mRNA expression levels. Mucosal inflammation symptoms correlated with increased levels of albumin, but not with increased levels of ECP, secreted proinflammatory cytokines or cytokine gene mRNA expression. We conclude that the symptoms are non-specific and do not correlate with occupational exposure to UV coatings under the conditions of this investigation.

Topics: Albumins; Biopsy; Chemical Industry; Cytokines; Eosinophils; Female; Gene Expression; Humans; Inflammation; Interleukin-8; Male; Nasal Cavity; Nasal Lavage Fluid; Occupational Diseases; Occupational Exposure; Paranasal Sinus Diseases; Pharyngeal Diseases; RNA, Messenger; Tumor Necrosis Factor-alpha; Wood

Fronto-ethmoidal mucocoeles have the capacity to destroy bone. Sinus lining tissue has been obtained at surgery from patients with mucocoeles, from those with chronic sinusitis undergoing endoscopic sinus surgery and from patients undergoing craniofacial resection. Tissues have been frozen, sectioned, and subjected to immunohistochemical examination with monospecific antibodies for the presence of the potent osteolytic cytokines interleukins-1 and -6 and tumour necrosis factor alpha. In addition, the chemotactic intercrine--interleukin-8 was investigated. The presence of the cytokine-inducible vascular endothelial adhesion receptors--Inter-Cellular Adhesion Molecule (ICAM)-1 and E-Selectin (also known as Endothelial Leukocyte Adhesion Molecule--ELAM) was also determined. Normal sinus tissue showed no immunoreactivity with the antibodies to these various moieties. Surprisingly, only a small proportion of tissues from patients with chronic sinusitis showed the presence of cytokines or vascular adhesion receptors. In contrast, all specimens of fronto-ethmoidal mucocoeles showed positive staining for IL-1 alpha and beta and for ICAM-1 and E-selectin. IL-1 immunostaining was restricted to the epithelial cell population not being found in infiltrating leukocytes. In 40% of mucocoeles infiltrating macrophage-like cells showed the presence of tumour necrosis factor alpha. The presence of the potent osteolytic cytokine--IL-1 in all specimens of fronto-ethmoidal mucocoeles coupled to the finding of the IL-1-inducible adhesion molecules ICAM-1 and E-Selectin argues strongly that IL-1 is released from the epithelial cells and that this cytokine may be the factor causing the erosion of bone overlying the expanding mucocoele. The nature of the signals inducing cytokine synthesis remain, however, unidentified.

Topics: Adult; Aged; Antigens, Differentiation, Myelomonocytic; Cell Adhesion Molecules; Chemotactic Factors; Cytokines; E-Selectin; Ethmoid Sinus; Female; Frontal Sinus; Humans; Intercellular Adhesion Molecule-1; Interleukin-1; Interleukin-6; Interleukin-8; Macrophages; Male; Membrane Glycoproteins; Middle Aged; Mucocele; Mucous Membrane; Paranasal Sinus Diseases; Platelet Endothelial Cell Adhesion Molecule-1; Receptors, Immunologic; Sinusitis; Tumor Necrosis Factor-alpha